Abstract
We examined the possible involvement of connective tissue growth factor (CTGF) in the apoptosis induced by transforming growth factor-beta(1) (TGF-beta(1)) in human aortic vascular smooth muscle cells (HASC). In quiescent HASC, TGF-beta(1) induced the mRNA and protein of CTGF. A CTGF antisense oligonucleotide inhibited this induction. TGF-beta(1) significantly reduced cell viability and induced DNA fragmentation, and the CTGF antisense oligonucleotide reversed these effects. Moreover, TGF-beta(1) activated caspase 3 in HASC, and the CTGF antisense oligonucleotide reduced this activation. These findings show that CTGF plays a key role in the TGF-beta(1)-induced apoptosis in HASC.
MeSH terms
-
Aorta / cytology
-
Aorta / drug effects
-
Apoptosis / drug effects*
-
Caspase 3
-
Caspases / metabolism
-
Cell Survival / drug effects
-
Cells, Cultured
-
Connective Tissue Growth Factor
-
DNA Fragmentation / drug effects
-
Enzyme Activation / drug effects
-
Growth Substances / genetics
-
Growth Substances / physiology*
-
Humans
-
Immediate-Early Proteins*
-
Intercellular Signaling Peptides and Proteins*
-
Muscle, Smooth / cytology
-
Muscle, Smooth / drug effects*
-
Oligodeoxyribonucleotides, Antisense / genetics
-
Oligodeoxyribonucleotides, Antisense / pharmacology
-
RNA, Messenger / drug effects
-
RNA, Messenger / genetics
-
RNA, Messenger / metabolism
-
Transforming Growth Factor beta / pharmacology*
Substances
-
CCN2 protein, human
-
Growth Substances
-
Immediate-Early Proteins
-
Intercellular Signaling Peptides and Proteins
-
Oligodeoxyribonucleotides, Antisense
-
RNA, Messenger
-
Transforming Growth Factor beta
-
Connective Tissue Growth Factor
-
CASP3 protein, human
-
Caspase 3
-
Caspases